Researchers at University Hospital of Wales, Cardiff; and University of Bristol, UK studied the clinical features and disability in pediatric-onset multiple sclerosis (POMS) in a population-based cohort with long-term follow-up, and compared to a cohort of patients with adult-onset (AOMS) disease. Of 2068 patients identified with MS since 1985, 111 (5.4%) had POMS and in 110, disease onset was relapsing. Age of onset ranged from 4 to 17 years (mean, 15 years). Initial most frequent manifestations were motor in 52.8% and optic neuritis in 26.4%. No significant differences in sex ratio, familial recurrence, relapse rate, ethnicity or clinical symptoms at presentation were identified between POMS and AOMS. Compared to AOMS, POMS cases had a longer interval to second relapse (5 vs 2.6 years, p=0.04), less common primary progressive disease (0.9% vs 8.5%, p=0.003), longer time to develop secondary progressive disease (32 vs 18 years, p=0.0001), and longer to reach disability milestones (p < 0.0001). Incomplete recovery from initial event was significantly associated with a shorter time to reach disability milestones (p=0.01). Patients with POMS become disabled at a younger age and have a poorer age-related prognosis than AOMS cases. 
COMMENT. While prognosis of POMS appears more benign than that of AOMS in early disease, later stages of the disease are similar to AOMS and lead to an earlier disability.
Fibronectin Aggregation and Remyelination in MS
Researchers at Universities of Groningen and Amsterdam, The Netherlands, and Universities of Cambridge and Edinburgh, UK examined the expression of the extracellular matrix molecule fibronectin on demyelinating injury and how this affects remyelination by oligodendrocytes progenitors. In lesions undergoing remyelination, fibronectin expression was transiently increased in demyelinated areas and declined as remyelination proceeded. In chronically demyelinated MS lesions, fibronectin expression persisted as aggregates, resistant to degradation. Fibronectin aggregates within MS lesions contribute to failure of remyelination and are potential therapeutic targets for promoting remyelination.